Chapter 20 - Toxicity of ZnO nanoparticle-induced reactive oxygen species and cancer cells

Abstract

Recent studies have proved that zinc oxide (ZnO) nanoparticles can cause toxicity in different cell lines, and oxidative stress is often hypothesized to be an important factor in the cytotoxicity of ZnO nanoparticles. However, the mechanisms are incompletely understood. This chapter is aimed at investigating the role of oxidative stress in toxicity and possible involvement of mitochondria in the production of reactive oxygen species (ROS) upon exposure of retinal ganglion cells (RGC-5) to ZnO nanoparticles. The effects of ZnO nanoparticles on mitochondrial membrane potential and ROS levels involved in hydrogen peroxide and hydroxyl radical production were investigated via inverted fluorescence microscope and hydrogen peroxide and hydroxyl radical assay kits, respectively. The studies indicated that ZnO nanoparticles could apparently decrease the mitochondrial membrane potential, increase the production of ROS and lead to the overexpression of caspase-12 in RGC-5 cells, suggesting that ZnO nanoparticle-induced toxicity via ROS overproduction will trigger endoplasmic reticulum stress, lead to RGC-5 cell damage, and finally induce apoptosis/necrosis; the overexpression of caspase-12 may also be involved in cell death in RGC-5 cells. The studies suggest that widespread application of ZnO nanoparticles should be carefully assessed at the in vivo level for potential adverse biological effects.